Rupture of the Heart

pain which radiated to the neck. A diagnosis of angina pectoris was made, and appropriate treatment was started. Eleven hours later the patient was found dead in bed. Autopsy revealed a pericardium filled with 300 cc. of blood. In the anterior wall of the left ventricle there was a rupture of myocardium 1 cm. long, with two smaller pinpoint openings on each side of it. The rupture had occured in the center of a large area of recent myocardial infarction, the result of occlusive thrnombt in the anterior descending branch of the left coronary artery. The aorta and both coronarv nrteries ehowed atherosclerosis.

In the last two years, in 147 patients with malignant melanoma, we performed the "continuity" operation in 34 cases; 23 are still alive without evidence of disease and three are living with residual melanoma. Of six patients undergoing radical amputations, four are living without evidence of disease, and two are alive with recurrent melanoma.

SUMMARY AND CONCLUSIONS
We have presented an analysis of 862 cases of malignant melanoma, of which 595 were available for five-year end-result study, with an over-all salvage of 9.7 per cent. Radiation therapy alone in all its forms and combinations has yielded no fiveyear survivals. Surgical attack has resulted in 38. 4 per cent three-year and 17.7 per cent five-year salvage for localized melanomas, and 18.7 per cent three-year, and 15.6 per cent five-year salvage of patients with melanoma metastatic to regional lymph nodes. In addition, we have presumptive evidence of a trend toward greater saving of life by widening the scope of our radical surgical attack through the institution of one fundamental principle of cancer surgery, namely, the en masse excision of the primary lesion with its entire lymphatic drainage basin and the dissection of the regional nodes, "in continuity." Mason: The Principle of Excision and Dissection in Continuity for Primary and Metastatic Melanoma of the Skin, Surgery, 17:8494866 (June), 1945.
Rupture of the Heart WALTER W. ELLWOOD,* M.D., San Leandro CARDIAC failure is a condition which may kill a person instantly.2 Such sudden failure may be due to a thrombosis of a coronary artery, rupture of the interventricular septum,1 rupture of the ventricles, or hypertension with myocardial failure. Myocardial infarction results from ischemic necrosis of heart muscle. The necrotic muscle is gradually removed and replaced first by open granulation tissue rich in vessels, and later by fully formed sear tissue. This scarring of necessity develops slowly from the periphery of the necrotic area, leaving a central area of flabby, necrotic tissue which has very little tensile strength. The weakened area may give way and bulge outward so that aneurysm of the heart is formed with marked thinning of the wall, and rupture may occur through the center of the necrotic tissue. Rupture of the left ventricle through a recent infarct is unusual4 but may occur, particularly when the necrosis of the muscle is at its height and before significant replacement by scar tissue has taken place. It leads to very rapid death by cardiac tamponade, but if the tear is very small, bleeding may be so gradual that death is delayed for hours.
Friedman and White5 found ten cases of cardiac rupture in 270 instances of myocardial infarction among nearly 3,000 autopsies at the Massachusetts General Hospital. All were found in patients with acute infarction. However, in a series of cases of patients in mental institutions, Jetter and White6 report an incidence of 73 per cent of rupture of the Resident in Medicine, Fairmont Hospital of Alameda County.
heart with cardiac tamponade in cases with recent myocardial infarction. In spite of the fact that rupture of the heart is not a rare condition, many physicians and coroners still neglect to consider this condition as a cause of death, and are usually satisfied with a customary diagnosis of coronary heart disease or hypertension with myocardial failure.
This fact was admirably brought out by Simberge and Levine7 who pleaded for a more accurate appraisal of all sudden deaths attributed to heart disease. Correct diagnosis can be obtained in only one way: all physicis and _oroners should insist on postmortem examinations in every case of sudden death, and if no adequate cause is determinable by examination of the chest and abdomen, then the skull should be opened and the brain carefully examined. This will obviate the common practice of routinely signing a death certificate giving apoplexy or coronary occlusion as the cause of death.
Rupture of the heart with or without classical signs or symptoms suggesting myocardial infarction is a condition which the general practitioner either believes does not exist or which is so rare that it can be overlooked entirely as a cause of sudden death. Yet, in cases of sudden death, postmortem examination will not infrequently disclose a rupture of one of the ventricles through the area of a recent infarction. Clinical symptoms may be entirely lacking as in those cases of so-called "silent coronary." That this condition is far from rare is evidenced by the following four case reports of patients who died suddenly, with autopsy revealing rupture of the anterior surface of the left ventricle.
The four deaths occurred within a short period of time.
Case1.-An elderly, emaciated white male 81 years old entered the hospital in August, 1942, with a diagnosis of arteriosclerotic heart disease, senility, chronic bronchitis, and hemorrhoids. The hemorrhoids were treated by a series of injections with excellent results. Six months later the patient complained of bladder distress. Cystoscopy revealed a normal bladder. The only complaints in 1943 were bladder distress and constipation. In 1944, internal hemorrhoids were injected. Signs of increasing senility appeared in 1945, but otherwise the patient's condition was fair until the night of March 28-29, 1946, when he was restless in bed. At 6:15 a.m. on March 29 the patient was found dead in bed. Autopsy revealed an old healed infarct in the left ventricle, and at the apex on the anterior surface there was a rupture of the myocardium 1 cm. in length with 200 cc. of blood in the pericardial sac. The kidneys showed chronic interstitial nephritis, the liver, chronic passive congestion. The lungs were anthracotic and there was minimal sclerosis of the aorta. Microscopic examinalion revealed hemorrhage into and degeneration of the muscle fibers of the heart with a mixture of white blood cells infiltrated through all layers of the heart wall-'findings typical of a recent myocardial infarction. with 58 per cent hemoglobin; white blood cell count 4,800 with 71 polys, 22 lymphocytes, 5 monocytes and 2 basophiles. There were a few stippled red cells. The Kline was negative. X-rays showed good alignment of the bony fragments, with the Neufeld pin in place. The anemia was treated with ferrous sulphate, but because of a resultant diarrhea it had to be discontinued. Treatment consisted of active and passive movements of the left leg, bed rest and nursing care. The patient's progress was excellent until the night of July 2-3 when she became very restless and got out of bed three times but was returned to bed each time with no complaints. A short time later, at 5:40 a.m. on July 3, 1946, the patient was found dead on the floor beside her bed. Autopsy revealed a rupture 3 cm. long in the anterior surface of the left ventricle with hemopericardium. The aorta and aortic valve showed atherosclerosis. The coronary arteries were sclerosed but patent at the ostia and there was evidence of a recent myocardial infarction. There were no rales in the chest, but increased breath sounds and dullness were noted in the lower left lung field and at the right lung. Examination of the heart revealed frequent extrasystoles but no murmurs. A diagnosis of bronchio-pneumonia of the left lower lobe was made, the patient was put to bed and a course of sulfadiazine was started. His condition improved rapidly, the e Dr. T. R. Stepman, Assistant Resident In Medicine, Fairmont Hospital, assisted the author in the clinical chest pain disappeared and on the third day the patient was up and around and returned to his duties in the barber shop. An electrocardiogram taken June 13, 1946, showed a coving effect of the S-T segment in all leads. A diagnosis of recent coronary occlusion with evidence of myocardial damage was made. However, the patient insisted that he felt well, and he could not be kept in bed. At1 p.m. on June 14, the author saw the patient walking on his crutches about the hospital grounds. Two hours later, the patient became very dyspnoeic, was cyanotic, and showed some twitchings of the body. He was pronounced dead at 3:10 p.m. At autopsy, both lungs showed marked passive congestion. The pericardium contained 100 cc. of blood. All valves were normal. The aorta and both coronary arteries showed a moderate degree of atherosclerosis. On the anterior wall of the left ventricle there was an area about 2 by 2 cm. of thin, friable, bulging heart muscle, the site of the recent infarction of May 31. Below this area was a fresh infarct measuring 3 by 3 cm. and consisting of hemorrhagic, friable, and bulging heart muscle. The center of this second area was separated for a distance of 1.5 cm. and a fresh blood clot extended through this ruptured area from within the ventricle outward into the pericardial sac. which lasted a few minutes and then disappeared entirely. These convulsions recurred at long intervals during the next three years. In August, 1946, two small draining sinuses were found over the sacrum. The patient remained a nursing problem because of the old hemiplegia and the two draining sinuses. On October 10, 1946, she suddenly developed substernal pain which radiated to the neck. A diagnosis of angina pectoris was made, and appropriate treatment was started. Eleven hours later the patient was found dead in bed. Autopsy revealed a pericardium filled with 300 cc. of blood. In the anterior wall of the left ventricle there was a rupture of myocardium 1 cm. long, with two smaller pinpoint openings on each side of it. The rupture had occured in the center of a large area of recent myocardial infarction, the result of occlusive thrnombt in the anterior descending branch of the left coronary artery. The aorta and both coronarv nrteries ehowed atherosclerosis. COMMENT The first two cases disclosed rupture of the left ventricle due to a recent infarction, yet clinically no symptoms presented themselves. Therefore, the true diagnosis was established only by a careful autopsy examination. The third case was most interesting in that a diagnosis of coronary insufficiency was made antemortem, yet the patient was asymptomatic and refused to stay in bed. Substernal pain was absent and the patient was able to get around on his crutches and perform his usual duties as a barber. Then, 15 days later, the myocardium ruptured through an area of a second infarct below an already weakened part of the ventricle which showed a definite aneurysm of the heart wall. Cas'e four also had antemortem coronary insufficiency and developed a rupture through the site of a new infarction. Examination revealed the study and autopsy of Case 3. RUPTURE OF THE HEART 289 SUMMARY 1. Rupture of the heart following a recent myocardial infarction is a far from rare cause of acute cardiac failure. Signs and symptoms of the underlying myocardial infarction are sometimes entirely lacking.
2. Four cases are presented, in two of which no symptoms of coronary insufficiency were present.
The other two cases gave a definite history of cardiac distress. In one case (Number 3) an area of rupture of the heart was noted in a new area of infarction 15 days after an earlier infarction had already weakened the heart muscle and produced an aneurysm of the heart wall.
3. A plea of routine postmortem examinations is made in all cases of sudden death. This will obviate the practice of routinely signing death certificates in these cases with the causes listed as apoplexy, coronary thrombosis, or heart failure due to hypertension.